Abstract 80: Development of CA1 Damage: Different Cell Counts in CA1 Region of Rats Resuscitated from 8-Minute Ventricular Fibrillation Cardiac Arrest After 2 Weeks of Survival Compared with 20 Weeks of Survival

Abstract

Background: Rodent models of cardiac arrest (CA) help to investigate mechanisms and therapy of cerebral ischemia and reperfusion. The CA1 region of hippocampus is specifically vulnerable to global ischemia and is considered to play an important role in neurological deficits of patients surviving cardiac arrests. Methods: Male 350g Sprague-Dawley rats were put into ventricular fibrillation (VF) CA. After 8 min of CA the animals received mechanical chest compressions for 2 min and epinephrine 20 μg/kg. The animals were defibrillated thereafter every 2 min to achieve return of spontaneous circulation. Six animals surviving with favorable neurologic recovery were sacrificed after 2 weeks and 11 after 20 and compared to 4 sham rats. For histological examination brains were fixed in formalin, paraffin-embedded and cut into coronary sections of 3 μm thickness. In Hematoxylin- Eosin-stained sections viable neurons were counted in a 500 μm sector of the CA1 region. Results: In sham animals 84±12 viable cells were counted in CA1 region. Two week survivors had 16±8 cells (p< 0.001), whereas 20 week survivors had 37±31 (p=0.018 vs sham, p=0.084 vs 2 weeks survivors) cells. The latter showed in 7 animals many viable cells (60±15) compared to 2 weeks survivors and in 4 animals very few cells 4±3 cells. Conclusions: A repopulation within week 2 and 20 of pyramid cells in the CA1 region of the hippocampus seems to have taken place in 7 of 11 rats resuscitated from 8 min VFCA whereas in others not. To discover the mechanism responsible for this huge difference in cell counts of the CA1 region in long time survivors of CA might help to understand the pathological mechanisms of the global ischemic insult.